Module 3 - Gas exchange & immunity Flashcards

1
Q

When do Type 2 alveolar cells begin to produce surfactant?

A

~28-30 weeks gestation

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2
Q

What are the 4 types of hypersensitivity

A

Type 1 - IgE mediated allergies
Type 2 - IgM/IgG auto antibodies
Type 3 - antibody complexes
Type 4 - T-cell mediated –> macrophages/cytotoxic T-cells

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3
Q

What is bronchiolitis

A

acute lower respiratory tract infection
targets lung EPITHELIUM (not affected by bronchodilators)

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4
Q

Which virus typically causes bronchiolitis?

A

respiratory synctycial virus
other viruses: parainfluenza, mycoplasma, adenovirus

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5
Q

What age is bronchiolitis most common?

A

<2 years old

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6
Q

Respiratory anatomy of infants/children

A

narrow airway (funnel shaped, anterior facing)
narrowest part = cricoid making intubation difficult
immature intercostal muscles –> diaphragm primary mode of breathing
horizontal intercostal muscles –> rib cage moves up/down vs. up/out
abdominal breathing
obligate nose breathing until 6 months
shorter airway –> higher risk of lower respiratory infections
narrower lumen –> higher risk of obstruction

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7
Q

Types of retractions

A

tracheal tug
substernal
suprasternal
supraclavicular
intercostal
subcostal

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8
Q

Infant ventilation

A

extrathoracic airway narrow during inspiration and widen during expiration
inthrathoracic airway widens on inhalation and narrows on expiratoin
asymmetrical movement helps move air towards lungs

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9
Q

Extrathoracic definition

A

trachea

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10
Q

Intrathoracic

A

below trachea

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11
Q

Functional residual capacity

A

volume remaining in lungs after exhalation

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12
Q

Infant sleep & breathing

A

reduced gas exchange
reduced muscle tone –> narrower airway
shorter exhalations = increased functional residual capacity (reduced G/E)r
reduced intercostal activity

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13
Q

Intermittent breathing

A

normal for infants to stop breathing for up to 15 seconds

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14
Q

True infant apnea

A

no breathing for >20 seconds

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15
Q

Restrictive lung disorders

A

pulmonary edema
respiratory distress syndroem

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16
Q

Obstructive lung disorders

A

asthma
allergies?

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17
Q

Croup sounds

A

stridor on inspiration

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18
Q

Asthma sounds

A

prolonged expiration, wheezing

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19
Q

Cortisol and surfactant

A

increase maturation of Type 2 alveolar cells & increase surfactant production

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20
Q

Insulin and surfactant

A

decrease production fo surfactant

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21
Q

URTI

A

inflammation of upper airway –> impacts inspiration

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22
Q

LRTI

A

inflammation of lower airways –> impacts expiration
*air trapping, prolonged expiration

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23
Q

URT anatomy

A

nose
mouth
sinuses
larynx

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24
Q

LRT anatomy

A

trachea
bronchi
bronchioles -> alveoli
lungs

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25
S/S impending respiratory failure
increased WOB retractions grunting reduced chest movement cyanosis not relieved by O2 therapy HR >150 OR increasing/decreasing bradycardia tachypnea or bradypnea extreme anxiety/agitation fatigue reduced LOC
26
Bronchiolitis Treatment
1)O2 therapy (humidifed) 2)hydration (IV, NG) other: positioning (elevate head) reduce fatigue nasal suction (infants) epinephrine/dexamethasone
27
Syncytia
merging of epithelial cells d/t RSV
28
CD8 T-cells
differentiate into cytotoxic T-cells
29
CD4 T-helper cells
TH1 --> stimulate cytotoxic T-cells TH2 --> stimulate B-cells to differentiate into plasma cells. Promote class switching
30
Which T-helper cell is more commonly associated to allergies?
TH2 *TH2 shift occurs in pregnancy --> more prone to developing allergies
31
Mechanism of TH1 hypersensitivity
APC presents antigen to TH2 --> TH2 cells rls mediators that cause B-cells to differentiate into IgE producing cells IgE antibodies bind to allergen IgE antibodies bind to mast cells via Fc region --> PRIMING on secondary exposure, allergen crosslinks IgE antibodies on mast cell surface cause mast cell degranulation --> allergic symptoms
32
Where are mast cells located?
connective tissue skin mucous membranes adjacent to blood/lymph vessels
33
Where are basophils located?
bloodstream
34
Type 1 phases
Primary/immediate --> mast cells Secondary/late --> inflammatory cells sustain inflammation
35
Mechanism of Type 2 hypersensitivity
IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface 1) complement/antibody mediated cell destuction 2) " inflammation 3) antibody-mediated cellular dysfunction
36
Mechanism of Type 2 hypersensitivity
IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface 1) complement/antibody mediated cell destuction 2) " inflammation 3) antibody-mediated cellular dysfunction
37
Types of T2 hypersensitivity reactions
blood transfusion reactions hemolytic disease of newborn
38
Virus components
genetic material --> DNA or RNA protein capsid envelope (cell membrane attached to virus --> OPTIONAL)
39
What type of virus evolves more rapidly?
RNA
40
Bronchiolitis patho
epithelial inflammation pulmonary edema increased mucus production ---> mucus plug tissue necrosis
41
What is asthma?
chronic obstructive respiratory disease that causes airway inflammation, edema, mucus production and bronchospasm
42
Common asthma triggers in children
viral RTI allergens air pollution seasonal changes reduced medication compliance
43
PRAM
pediatric respiratory assessment measure
44
Asthma treatment
bronchodilators anticholinergics systemic corticosteroids O2 therapy magnesium sulfate (relax smooth muscle) IV drugs intubation/ventilation Bipap/CPAP
45
Asthma & breathing
a lack of wheezing/silent chest can indicate the airway was completely closed and respiratory failure is imminent
46
PRAM scores
mild 0-3 moderate 4-7 severe 8-12
47
Asthma symptoms
1) dyspnea, chest tightness, wheezing, sputum production, and cough, 2) airflow obstruction (s/t inflammation) 3) bronchial hyperresponsiveness (IgE mast cells) 4) underlying airway inflammation
48
Types of asthma
atopic non-atopic
49
Atopic asthma
type 1 hypersensitivity reaction caused by IgE antibodies responding to allergens
50
Non-atopic asthma
non-allergenic asthma. caused by triggers such as viral infection, stress, pollution, exercise, etc.
51
Systemic effects of corticosteroids
adrenal suppression growth impairment decreased bone density myopathy weight gain
52
Layers of respiratory tract
mucosa (epithelium + lamina propria) submucosa basement membrane cartilage/smooth muscle/adventitia
53
How does aspirin promote asthma?
aspirin = nsaid inhibition of COX pathway leads to increased LOX activation increased LOX = increased immune response --> hyperreactivity
54
Long-term effects of asthma
smooth muscle & goblet cell hypertrophy injury to epithelium blood vessel proliferation
55
Asthma phases
Early phase 10-20 onset caused by IgE antibodies Late phase 4-8 hrs post exposure -> inflammatory cells rls mediators prolonging inflammation
56
Leukotrienes & inflammation
bronchoconstriction increased bronchial reactivity mucosal edema mucous hypersecretion
57
How do infants breath
extrathoracic airway narrows on inspiration, widens on expiration intrathoracic airway widens on inhalation, narrows on expiration
58
Incubation of RSV
2-8 days
59
Stages of extrinsic asthma
1) sensitization 2) provocation
60
Phases of an asthma attack
early (within minutes d/t IgE antibodies) late (hours d/t rls of inflammatory cells/mediators)